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Query: UMLS:C0038187 (
starvation
)
24,951
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
This study was carried out to test the hypothesis that reduced hypothalamic GnRH release is responsible for the suppression of reproductive functions during
starvation
. Adult male rats were kept for 4 days under total fasting (only water allowed) and injected during this time at 2-h intervals with 100 or 500 ng/kg BW of GnRH or vehicle. Serum levels of LH and
FSH
decreased by 30% during
starvation
(p less than 0.05), and these effects were fully reversed by either dose of GnRH treatment.
Starvation
reduced the pituitary mRNA contents of the gonadotropin common alpha- and
FSH
beta-subunits by 30% and 35% in starved animals (p less than 0.05 for both), but the LH beta-subunit mRNA was unaffected. The GnRH treatments partly or totally reversed these changes, but up-regulation of the mRNA levels by GnRH was seen only in controls fed ad libitum.
Starvation
reduced the testicular and serum levels of testosterone by 84% (p less than 0.01) and 42% (p less than 0.05), respectively. These changes were fully reversed by the 500-ng/kg dose of GnRH treatment during fasting, but only serum T was completely reversed by the 100-ng/kg GnRH treatment. To elucidate whether fasting per se had direct effects at the gonadal level, we blocked the secretion of gonadotropins by treatment with a GnRH antagonist, and replaced the gonadotropins by injecting of hCG (10 IU/kg BW once daily) and hFSH (75 IU/kg BW once daily). No differences were observed between starved and control animals in either testicular or serum levels of T, or in accessory sex gland weights.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Starvation-induced suppression of pituitary-testicular function in rats is reversed by pulsatile gonadotropin-releasing hormone substitution. 190 39
This paper discusses hormonal and metabolic reactions of healthy volunteers exposed to 14-day
starvation
. This exposure led to many-fold increase of plasma and urinary epinephrine (E); drastic increase of ACTH and beta-endorphin (BE), morning and integrated concentrations of cortisol and STH, aldosterone, T3, glucagon, cAMP, cGMP, cAMP-cGMP, acetyl choline (AC), free fatty acids (FFA), lactate, metanephrine (MN) excretion; decrease of plasma norepinephrine (NE) and unchanged NE excretion; decrease of plasma concentrations of TTH, T4, T3, prolactin (PL), insulin (morning and integrated concentrations), C-peptide,
FSH
, LH, testosterone, histamine, prostaglandins (PG) A + E, PG F2, glucose and pH, as well as decrease of excretion of homovanillic acid (HVA), vanillyl mandelic acid (VMA), normetanephrine (NMN) and MN-E, NMN:NE. On recovery day 14 concentrations of E, NE, BE, STH, AC, cAMP, cGMP, FFA as well as E and dopamine excretion remained elevated while concentrations of T3, PL, FT, LT, testosterone PG A + E, PG 2 and excretion of MN, HVA, VMA, MN:E remained decreased, while other parameters returned to the normal.
...
PMID:[Hormonal and metabolic reactions in the human body during prolonged starvation]. 237 73
Two hypotheses have been postulated as to the pathogenesis of hypogonadotropinemia in anorexia nervosa; one is
starvation
and weight loss and the other is a psychological factor to influence gonadotropin secretion. Our patient suffered from very rare concurrence of Turner's syndrome and anorexia nervosa and a study of this experiment in nature provided important evidences concerning decreased secretion of gonadotropins in the eating disorder. The patient was diagnosed as Turner's syndrome when she was 6 years old. Her gonadotropin levels were elevated to the castrated ranges (LH 61.8 IU/l;
FSH
175.8 IU/l) after 8 years of age. She was noticed to be anorectic at the age of 13 years. Serum levels of the pituitary gonadotropins were lowered (LH 2.9 IU/l;
FSH
3.0 IU/l) and their responses to luteinizing hormone-releasing hormone were decreased beneath the normal prepubertal limits. After one year of the anorectic period, she recovered the weight though her gonadotropin levels remained in the very low ranges (LH 2.7 IU/l;
FSH
2.5 IU/l). The results suggest that hypogonadism in anorexia nervosa is not solely caused by nutritional deficiency but rather by other factors such as psychological abnormalities.
...
PMID:Prolonged suppression of gonadotropin secretion after weight recovery in an anorectic patient with Turner's syndrome: reduced gonadal function in anorexia nervosa is independent in part on nutrition. 251 41
To investigate the role of the dopaminergic system in the pituitary adaptation to energy deprivation, the effect of metoclopramide, a dopamine receptor blocker, on prolactin (PRL), TSH,
FSH
and LH secretion was investigated in 6 healthy men in the fed state and at 36 h
starvation
. All underwent a further 36 h of
starvation
on a separate occasion to assess the effect of
starvation
on the TSH and PRL responses to TRH and the LH and
FSH
responses to gonadotrophin releasing hormone (GnRH). In all subjects
starvation
produced the expected reduction in serum T3 and an average decrease of 53% in the cumulative TSH response to TRH. The basal serum PRL and its response to TRH and metoclopramide remained unchanged with 36 h
starvation
. The
FSH
response to GnRH also remained unchanged, but the LH response was significantly greater during
starvation
. We conclude that factor(s) other than dopamine influence not only thyrotrophic activity but also other aspects of pituitary function during energy deprivation.
...
PMID:Dopamine in the pituitary adaptation to starvation in man. 392 79
To test the effect of chronic
starvation
on gonadotrophin secretion and oestrous cycles, rats were fed 50% of their normal chow consumption for 16 days. This caused an increasing rate of anoestrus which became significant during the third expected cycle (6 of 10 rats, P less than 0.02) and increased to 8 of 10 rats (P less than 0.0001) between day 12 and 16. The accompanying weight loss was around 13 and 17%, respectively. Pituitary weights in intact rats killed on dioestrus became significantly different after 8 days of chow reduction (12.8 +/- 0.2 vs 11.3 +/- 0.4 mg, P less than 0.02) with further reductions in groups killed after 12 and 16 days. At this time dioestrous serum
FSH
levels were significantly increased in starved rats (112 +/- 16 vs 161 +/- 13 ng/ml, P less than 0.01), while serum LH levels decreased significantly after 12 days (25.0 +/- 3.4 vs 13.1 +/- 8.8 ng/ml, P less than 0.001).
Starvation
decreased the LH response to LRH administration compared to pro-oestrous controls (1934 +/- 672 vs 289 +/- 39 ng/ml, P less than 0.05), whereas the
FSH
response was not impaired (457 +/- 91 vs 336 +/- 54 ng/ml, P greater than 0.05). In contrast to this pituitary content of LH was similar in both groups, while
FSH
content was significantly higher in starved animals (13.6 +/- 1.7 vs 19.8 +/- 1.2 micrograms, P less than 0.01). Chronic
starvation
immediately after ovariectomy did not affect the post-castrational rise of gonadotrophins. However, LRH administration caused higher serum
FSH
levels in starved rats (1540 +/- 91 vs 1833 +/- 90 ng/ml, P less than 0.05), whereas LH values did not differ (908 +/- 192 vs 721 +/- 153 ng/ml, P greater than 0.05). Gonadotrophin content per pituitary in castrated rats after 16 days of
starvation
was unchanged.
...
PMID:Starvation induced anoestrus: effect of chronic food restriction on body weight, its influence on oestrous cycle and gonadotrophin secretion in rats. 641 20
We have found high affinity binding of insulin not only in rat liver and kidney, but also in testis and male sex accessory tissues, prostate, seminal vesicle, and epididymis. We have studied particularly the characteristics of insulin binding in the testis. Membranes sedimenting at 100,000 X g showed the highest binding after 6-20 h of incubation at 0 C. Higher temperatures (15 and 25 C) resulted in lower binding. More than 90% of membrane-bound radioactivity after long incubations at 0 C was eluted at the same position as insulin by Sephadex G-50 chromatography. Membranes could be stored at -80 C for several weeks without loss of activity. Studies on binding specificity showed the following order of competition relative to insulin (100): desalanine insulin (84), proinsulin (2), and desoctapeptide insulin (1). Other peptidic hormones, LH,
FSH
, PRL, GH, glucagon, and ACTH-(1-24) were totally ineffective. Scatchard representation of the binding data could be resolved into two components with respective affinity constant (Ka) of 1.6 X 10(9) M-1 and 3 X 10(6) M-1. Testicular high affinity binding in adult rats did not vary after 3 days of
starvation
. However, it increased with age from 1-6 months. By contrast, in rat liver, this type of binding increased after
starvation
but decreased slightly at 6 months of age. These results show that testicular insulin receptors are similar to those of the liver but may have a different physiological control.
...
PMID:Specific insulin binding sites in rat testis: characterization and variation. 703 Jul 19
Testosterone (T) inhibits the synthesis and secretion of
FSH
and LH by decreasing the secretion of GnRH from the hypothalamus. However, T is also able to stimulate
FSH
gene expression and synthesis at the pituitary level when the release or action of GnRH is blocked. In the present study, we analyzed whether the positive effect of T on pituitary
FSH
could also be brought about during food restriction, which represents a model of suppressed GnRH secretion. We also wanted to learn whether this positive effect could be detected if GnRH pulsatility is maintained by exogenous injections. Adult male rats were subjected to various combinations of the following treatments: 1) implantation of silastic capsules containing T for Days 0-4 of the experiment, 2)
starvation
for Days 1-4 of the experiment, and 3) GnRH-treatment at 2-h intervals (500 ng/kg BW) for Days 3-4. The combined treatments were as follows: 1) control, 2) only
starvation
, 3) only GnRH, 4) starvation+GnRH, 5) only T, 6) starvation+T, 7) GnRH+T, and 8) starvation+GnRH+T (n = 12/group; two independent experiments). Serum
FSH
level was decreased 20% by
starvation
(p < 0.01), but no decrease was observed when the starving animals were treated with T. GnRH treatment increased serum
FSH
in both ad libitum-fed and starving animals to 266% and 333% of the respective control values (both p < 0.01). When T was added to these treatments, the increases in serum
FSH
were smaller, 219% and 272%, respectively (p < 0.01 vs. respective groups without T).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Modulation of gonadotropin secretion at the pituitary level by testosterone in gonadotropin-releasing hormone-treated male rats during food deprivation. 778 2
Short-term
starvation
suppresses the pituitary-testicular function in rats, evidently through inhibition of gonadotrophin-releasing hormone (GnRH) release. However, when gonadotrophin secretion is strongly enhanced, e.g. after castration,
starvation
does not suppress gonadotrophins. To test whether the time since castration affects the pituitary response to
starvation
, adult male rats were totally deprived of food for five days (only water allowed) immediately (acute castration) or two weeks after castration (chronic castration). The pituitary contents of GnRH receptors were decreased by
starvation
in sham-operated animals, unaffected in acutely castrated rats, but increased in chronically castrated animals, in comparison with appropriate controls (P < 0.01). Castration per se increased steady-state mRNA levels of the common alpha-chain and the LH and
FSH
beta-chains in all groups studied. The only consistent effect of
starvation
on these parameters was the 1.7 to 2-fold increase in the pituitary content of LH beta-subunit mRNA in acutely and chronically castrated rats (P < 0.01).
Starvation
alone suppressed LH secretion, acute castration eliminated this effect, but in chronically castrated rats, the
starvation
effect was stimulatory.
Starvation
did not affect
FSH
secretion in sham-operated and acutely castrated rats, but after chronic castration, the effect was stimulatory. In conclusion, the overall effect of
starvation
on gonadotrophins shifts gradually after castration from suppression, in sham-operated rats, to stimulation, in chronically castrated animals. Parallel changes in pituitary GnRH receptors suggest similar changes in GnRH secretion. Hence,
starvation
has both negative and positive effects on the GnRH-gonadotrophin-axis. The negative effect is evidently androgen-dependent and dominates in testes-intact animals. After chronic castration, only the positive, non-androgen dependent, stimulatory effect remains.
...
PMID:The time since castration influences the effects of short-term starvation on gonadotrophin secretion in male rats. 782 86
Functional hypothalamic amenorrhea are frequently observed. Body weight, body composition, eating attitudes, exercise are potent modulators of gonadotrop axis. Animal studies and clinical observations stress the fact of a major impact on ovary function of
starvation
or caloric restriction, weight loss and fat mass deficiency, eating disorders, stress or high intensive exercise training. From a pathophysiological point of view, insulin, IGF's system, leptine and central neuromediators are a link between nutrition and the gonadotropic axis. Initial clinical evaluation may strongly suggest the environmental origin of the amenorrhea. Basal hormonal evaluation (gonadotropins, prolactin, androgens ...) excludes other diseases and specialised evaluations [basal metabolic rate (BMR), Free T3 ...] could confirm the diagnosis. A low BMR, and a low Free T3, a normal
FSH
level with a low LH level suggest the nutritional origin of the amenorrhea. Improvement of nutritional intake and body composition with a psychological follow up may reverse the gonadotropin deficiency. If this deficiency persists hormonal replacement therapy is added in order to prevent the short or long term consequences (osteoporosis) of hypoestrogenism.
...
PMID:[Nutritional hypogonadism]. 1048 60
Depriving the ovary of exogenous
FSH
for 1, 2 or 3 d following a bolus injection of
FSH
was shown to influence the quality of the recovered oocytes. Thus, we compared the developmental competence of oocytes from heifers which had been stimulated for 3 d with
FSH
(Folltropin-V) and, after an interval of 36, 48 or 60 h, underwent blind transvaginal aspiration. The ovaries of heifers with a palpable or functional corpus luteum were aspirated to remove all large follicles 2 d prior to being injected with either 6 doses of saline (S), 6 doses (20 mg/mL) of
FSH
(F), or in 6 decreasing doses of
FSH
(3, 3, 2, 2, 1, 1 mL; Fd). Follicles were counted and classified (medium: 5 to 10 mm, large: >10 mm) with ultrasonography before each aspiration. The oocytes recovered were classified, matured, fertilized, and developed in vitro. On a per animal basis, 1.5, 5.2 and 4.7 large and 1.5, 10.7 and 10.7 medium follicles were counted for S, F and Fd, respectively. A mean of 3.3, 9.1 and 7.7 oocytes was recovered for treatments S, F and Fd, respectively and 58, 94 and 82% were enclosed in a nonexpanded cumulus or a corona layer. Oocyte development rates were based on counts of embryos with 32 or more nuclei at Day 6.5. When oocytes were recovered 36 h after the last injection, an average of 1, 2.7 and 2 embryos per animal was obtained with S, F and Fd, respectively; at 48 h, 0.75, 4.25 and 1 embryo; and at 60 h, 0, 2.5 and 2.7 embryos. Variance analysis was performed, and the protected LSD test indicated that treatment F at 48 h resulted in a significantly higher embryo rate than Fd at 48 h (P<0.05) or S (all times; P<0.05). The reduced effect of the Fd regimen could be due to the decreasing
FSH
support during follicular growth or to the lower total amount of
FSH
given. In conclusion, these results indicate an advantage of using moderate (3 d) follicle stimulation followed by a period of
FSH
starvation
to obtain optimal embryo production.
...
PMID:The time interval between FSH administration and ovarian aspiration influences the development of cattle oocytes. 1072 95
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